Abstract

The concept of osteoimmunology is based on growing insight into the links between
the immune system and bone at the anatomical, vascular, cellular, and molecular levels.
In both rheumatoid arthritis (RA) and ankylosing spondylitis (AS), bone is a target
of inflammation. Activated immune cells at sites of inflammation produce a wide spectrum
of cytokines in favor of increased bone resorption in RA and AS, resulting in bone
erosions, osteitis, and peri-inflammatory and systemic bone loss. Peri-inflammatory
bone formation is impaired in RA, resulting in non-healing of erosions, and this allows
a local vicious circle of inflammation between synovitis, osteitis, and local bone
loss. In contrast, peri-inflammatory bone formation is increased in AS, resulting
in healing of erosions, ossifying enthesitis, and potential ankylosis of sacroiliac
joints and intervertebral connections, and this changes the biomechanical competence
of the spine. These changes in bone remodeling and structure contribute to the increased
risk of vertebral fractures (in RA and AS) and non-vertebral fractures (in RA), and
this risk is related to severity of disease and is independent of and superimposed
on background fracture risk. Identifying patients who have RA and AS and are at high
fracture risk and considering fracture prevention are, therefore, advocated in guidelines.
Local peri-inflammatory bone loss and osteitis occur early and precede and predict
erosive bone destruction in RA and AS and syndesmophytes in AS, which can occur despite
clinically detectable inflammation (the so-called 'disconnection'). With the availability
of new techniques to evaluate peri-inflammatory bone loss, osteitis, and erosions,
peri-inflammatory bone changes are an exciting field for further research in the context
of osteoimmunology.